The advent of immune checkpoint inhibitors has revolutionized cancer therapy by leveraging the body's immune system to combat malignancies effectively. Among these groundbreaking agents, programmed cell death protein 1 (PD-1) and programmed cell death ligand 1 (PD-L1) inhibitors have emerged as pivotal therapeutic approaches. PD-L1, a key protein expressed on the surface of various cells, including cancer cells, plays a central role in immune regulation by interacting with the programmed cell death protein 1 (PD-1) receptor on T-cells leading to immune suppression. The substantial increase in PD-L1 expression on cancer cell surfaces has driven the exploration of PD-1/PD-L1 inhibitors as potential immunotherapeutic agents. These inhibitors are monoclonal antibodies designed to impede the PD-L1 and PD-1 interaction and disrupt the immunosuppressive signal, thereby reinvigorating the anti-tumor immune response mediated by activated T-cells. Clinical trials investigating PD-1/PD-L1 inhibitors have demonstrated remarkable efficacy in the treatment of diverse advanced or metastatic cancers, including leukemia, non-small cell lung (NSCLC), hepatocellular, melanoma, gastric, colorectal, and breast cancers, among others. Regulatory approvals have been granted for both monotherapy and combination therapy with other cancer treatments, encompassing chemotherapy and additional immune checkpoint inhibitors. While PD-1/PD-L1 inhibitors have exhibited significant success, they are not devoid of challenges. The emergence of intrinsic or acquired resistance, as well as immune-related adverse events, warrants thorough investigation and management. Consequently, researchers have embarked on combination trials to augment the therapeutic potential of PD-1/PD-L1 inhibitors and surmount resistance mechanisms.

A medical condition known as alcohol use disorder (AUD) is defined as an impaired capacity to reduce or regulate alcohol consumption despite negative social, occupational, or health effects. According to studies, habitual drinkers experience a reduction in their capacity to process new information, gain new skills, and formulate plans. Studies indexed in PubMed, PubMed Central, Google Scholar, ResearchGate, and ScienceDirect, published from 2012 to 2022, were identified through the search terms “alcohol use disorder” and “executive function.” A total of 2242 abstracts were identified through the initial search terms. Full texts were reviewed for 61 articles, out of which nine articles met the criteria for inclusion. This systematic review was based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The current systematic review primarily focuses on the following issues: clinical neuropsychological tests of executive dysfunction, specific brain regions most affected by alcohol neurotoxic effects, and alcohol-related dementia. This review concluded that chronic alcohol dependence syndrome causes impairments in several cognitive function domains. Study shows frontal lobe damage is caused by chronic alcohol consumption. A faulty interaction among large-scale networks underlies patients' executive dysfunction in AUD, which is suggested by changes in prefrontal white-matter pathways. The goal of this systematic review is to improve the ability to recognize alcoholics who are particularly at risk of functional impairments to tailor therapeutic therapy to maximize the chance of maintaining abstinence and neuropsychology concerning this complex disease.

Obesity is a major health problem worldwide resulting in numerous health conditions such as heart disease, stroke, type 2 diabetes (T2D), and certain types of cancer which are among the leading causes of premature preventable deaths. Recently, glucagon like peptide-1 receptor agonists (GLP-1 RA) has been identified as the most promising intervention in treating obesity. Our systematic review aims to analyze the efficacy of semaglutide, a GLP-1RA in treating obesity. We searched PubMed, Science Direct, and Google Scholar databases to review and distill full-text articles based on the eligibility criteria and involved 12 papers of clinical trials. The review found that semaglutide is safe and effective in treating obesity, and complications reported were primarily gastrointestinal events. Further exploration with more number of clinical trials involving greater sample size and lengthier time of follow-up is essential to determine its efficacy and safety in a diverse group of individuals who are overweight or obese and the dose required along with the duration of treatment.

Targeting apoptosis in cancer therapy has become increasingly popular, and there has been an increasing debate on whether apoptosis should be one of the main targets of therapy in cancer management. This study demonstrates the definition of apoptosis, the signaling pathways, and the pathogenesis behind it. We also show the correlation between apoptosis and cancer and how cancer can evade apoptosis to develop resistance to therapy. In addition, we illustrate the efficacy of adding pro-apoptotic therapy to conventional radio-chemotherapy cancer treatment. A systematic review was conducted using PubMed, PubMed Central (PMC), and ResearchGate, including papers written in English, focusing on adult and geriatric populations, in literature reviews, systematic reviews, and randomized controlled trials published in the last 25 years with relevance to the question. Based on the findings of this review, we conclude that apoptosis is a very sophisticated programmed cellular death with many signaling pathways. Its evasion should be considered one of the hallmarks of cancer and is responsible for multiple drug resistance (MDR) to cancer therapy. Targeting apoptosis seems promising, especially if combined with radio-chemotherapy.

Irritable bowel syndrome (IBS) is a common pathology in middle-aged patients and a regular consultation in the gastroenterology office. The prevalence is high in females with a ratio of 2:1, and due to its multifactorial etiology, it is difficult to address the symptomatology. On the other hand, fibromyalgia syndrome (FMS) is a chronic widespread pain syndrome also prevalent in the female population, characterized by systemic symptoms. It is proven that 28-59 % of patients with FMS develop IBS at some point in their illness; on the other hand, 32-77% of those with IBS will develop FMS. Our study aims to compile information about the pathogenesis of these diseases and highlight their common processes to target these two illnesses potentially. This systematic review comprises twenty-three studies published between 2017 and 2022, selected by electronic research with keywords and Medical Subject Headings (MESH) strategy. The articles were taken from PubMed, Pubmed Central (PMC), Medline, and Cochrane libraries and met the inclusion and exclusion criteria and the pertinent quality checklists. Of the reviewed studies, 10 were case-control, six were narrative reviews, three were systematic reviews, three were cross-sectional, and one was a cohort study. They investigated the correlation and similitudes in the pathogenic process between FMS and IBS. There are some similar mechanisms in the physiopathologies of IBS and FMS, where the immune system, especially the mast cells (MCs), along with their products, receptors, the inflammatory cells with their intermediaries, hormones, and neurotransmitters such as serotonin, act together pathologically. Also, the role of the microbiota is very important in this pathogenesis since dysbiosis alters the levels of serotonin in the body and can produce hyperstimulation of the autonomic nervous system. There are common associated factors in IBS and FMS, with evident symptoms presented in both syndromes such as fatigue, pain, hypersensitivity, depression, anxiety, and others, that could be correlated in a certain way. After this systematic review, we can conclude that the most accepted theories of the common pathogenesis are the role of serotonin and MCs with their inflammatory biomarkers, which can affect different parts of the body producing the characteristic symptomatology. Moreover, other pathogenic mechanisms such as the involvement of microbiota and dysregulation of the gut-brain axis have shown promising results, and further investigation should be made to support their role.

Being one of the most prevalent progressive neurodegenerative disorders (falling second only to Alzheimer’s disease) with a clinical pattern affecting millions of lives all over the world, Parkinson’s disease (PD) has never failed to attract a formidable interest from the vast majority of neurologists and researchers worldwide. This review article will analyze the pathophysiology, etiology, genetics, and pathological stages of Parkinson’s disease with their corresponding clinical sequels. A review article was conducted using research databases including PubMed, PubMed Central, Springer, and Elsevier. The research articles reviewed using databases were written in English, German, Japanese, and Chinese and published within the preceding 50 years. Based on the article’s findings, we concluded that Parkinson’s disease is a progressive disorder with a variety of motor and non-motor symptoms that are influenced by a cascade of pathological neuronal abnormalities such as Lewy neurites and Lewy bodies that gradually build up with an eventual consequence of neurodegeneration of dopamine-secreting neurons. Multiple genetic mutations, pathophysiological events, and environmental factors act as the foundation to initiate that cascade.